Indeed, the role of SUMO in atherosclerosis is well-exemplified by the reduction in NO generation due to SUMOylation of the proatherogenic activator of transcription factor 3 (ATF3) or by its modulating properties on NLRP3 inflammasome activity, release of inflammatory cytokines, and expression of adherence molecules [84,113]. This evidence concerns the gene ATF3 and atherosclerosis.